Evidence map›Paper›PMID 30001913›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2018

Genetic Rescue Reverses Microglial Activation in Preclinical Models of Retinitis Pigmentosa.

Lijuan Zhang, Xuan Cui, Ruben Jauregui, Karen Sophia Park, Sally Justus, Yi-Ting Tsai, Jimmy K Duong, Chun-Wei Hsu, Wen-Hsuan Wu, Christine L Xu and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 23 citations in OpenAlex.

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  8. The phase changes of M1/M2 phenotype of microglia/macrophage following oxygen-induced retinopathy in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  9. Article
  10. Novel REEP6 gene mutation associated with autosomal recessive retinitis pigmentosa.Documenta ophthalmologica. Advances in ophthalmology · 2020
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 2 countries.

Lijuan ZhangShanxi Eye Hospital, affiliated with Shanxi Medical University, 100 Fudong St., Xinghualing, Taiyuan, Shanxi, China. Electronic address: zhanglj2004@163.com.
Xuan CuiTianjin Medical University Eye Hospital, Tianjin Medical University Eye Institute & Tianjin Medical University School of Optometry and Ophthalmology, Tianjin 300384, China; Jonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA; Tianjin Medical University Eye Hospital, Tianjin, China.
Ruben JaureguiJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA; Weill Cornell Medical College, New York, NY, USA.
Karen Sophia ParkJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA.
Sally JustusJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA; Harvard Medical School, Boston, MA, USA.
Yi-Ting TsaiJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA.
Jimmy K DuongDepartment of Biostatistics, Mailman School of Public Health, Columbia University Medical Center, New York, NY, USA.
Chun-Wei HsuJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA.
Wen-Hsuan WuJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA.
Christine L XuJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA.
Chyuan-Sheng LinDepartment of Pathology and Cell Biology, Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University Medical Center, New York, NY, USA.
Stephen H TsangJonas Children's Vision Care and the Bernard & Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia Stem Cell Initiative, Columbia University, New York, NY, USA; Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA; Department of Pathology & Cell Biology, Stem Cell Initiative (CSCI), Institute of Human Nutrition, College of Physicians and Surgeons, Columbia University, New York, NY, USA. Electronic address: sht2@columbia.edu.
Columbia University · USNewYork–Presbyterian Hospital · USColumbia University Irving Medical Center · USShanxi Eye Hospital · CNTianjin Medical University · CN

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Anil K Rustgi · 1985 to 2026
$115.3M
Instrumentation, Fabrication, and Design CoreP30EY019007 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Xin Zhang · 2010 to 2026
$12.9M
Toward mechanism- and gene-based therapies for retinal degenerationR01EY018213 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Stephen H Tsang · 2008 to 2026
$6.6M
Gene Silencing and Gene Editing in PhototransductionR01EY024698 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Stephen H Tsang · 2015 to 2026
$4.7M
Mechanistic Studies on Regenerative Medicine Approaches to Childhood BlindnessR01EY026682 · NEI · UNIVERSITY OF IOWA · PI BASSUK, ALEXANDER G, MAHAJAN, VINIT B · 2016 to 2019
$1.6M
Evaluating GWAS AMD Candidate Loci by Gene Editing in Human iPS CellsR21AG050437 · NIA · UNIVERSITY OF IOWA · PI BASSUK, ALEXANDER G, MAHAJAN, VINIT B · 2015 to 2016
$431k
NCI NIH HHS P30 CA013696NEI NIH HHS P30 EY019007NEI NIH HHS R01 EY018213NEI NIH HHS R01 EY024698NEI NIH HHS R01 EY026682NIA NIH HHS R21 AG050437
6 · The paper itself

Abstract

Microglia cells (MGCs) play a key role in scavenging pathogens and phagocytosing cellular debris in the central nervous system and retina. Their activation, however, contributes to the progression of multiple degenerative diseases. Given the potential damage created by MGCs, it is important to better understand their mechanism of activation. Here, we explored the role of MGCs in the context of retinitis pigmentosa (RP) by using four independent preclinical mouse models. For therapeutic modeling, tamoxifen-inducible CreER was introduced to explore changes in MGCs when RP progression halted. The phenotypes of the MGCs were observed using live optical coherence tomography, live autofluorescence, and immunohistochemistry. We found that, regardless of genetic background, MGCs were activated in neurodegenerative conditions and migrated beyond the layers where they are typically found to the inner and outer segments, where degeneration was ongoing. Genetic rescue not only halted degeneration but also deactivated MGCs, regardless of whether the intervention occurred at the early, middle, or late stage of the disease. These findings suggest that halting long-term disease progression may be more successful by downregulating MGC activity while co-administering the therapeutic intervention.

Indexed as

AnimalsCX3C Chemokine Receptor 1Disease Models, AnimalGenetic TherapyHumansMiceMicrogliaPhosphoric Diester HydrolasesRetinitis PigmentosaTamoxifenTomography, Optical CoherenceCX3C Chemokine Receptor 1Cx3cr1 protein, mousePhosphoric Diester HydrolasesTamoxifenCre recombinasegenetic diseasesmicroglia cellsPde6 mutationretinitis pigmentosa

Identifiers

PMID30001913
PMCPMC6094486
OpenAlexW2809293496

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.